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Persistent hexavalent chromium exposure impaired the pubertal development and ovarian histoarchitecture in wistar rat offspring
Author(s) -
Samuel Jawahar B.,
Stanley Jone A.,
Sekar Pasupathi,
Princess Rajendran A.,
Sebastian Maria S.,
Aruldhas Michael M.
Publication year - 2014
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.21810
Subject(s) - offspring , in utero , hexavalent chromium , endocrinology , medicine , oxidative stress , ovary , biology , estrous cycle , andrology , physiology , fetus , pregnancy , chemistry , chromium , genetics , organic chemistry
Hexavalent chromium (CrVI) is a highly toxic metal and a major environmental pollutant. Several studies indicate that CrVI exposure adversely affects reproductive function. We reported that maternal Cr exposure resulted in Cr accumulation in the reproductive organs of female offsprings. CrVI can cross the placental barrier and also can be passed through breastfeeding. The present investigation aimed to determine the persistent ( in utero through puberal period) CrVI exposure‐induced toxic effects on the reproductive functions of mother and the offspring. Induction of oxidative stress is one of the plausible mechanisms behind Cr‐induced cellular deteriorations. Mother rats exposed to CrVI showed reduced reproductive outcome, while the offsprings showed higher accumulation of Cr in ovary, altered steroid, and peptide hormones. Specific activities of antioxidant enzymes were decreased and associated with increased levels of H 2 O 2 , and lipid peroxidation. CrVI exposure also damaged the ovarian histoarchitecture in various age groups studied. CrVI exposure also delayed the sexual maturation. Results from the present investigation suggest that CrVI exposure from in utero through puberal period significantly damaged the pubertal development through altered antioxidants, anemia, and altered hormone levels. These changes were associated with damaged ovarian histoarchitecture and extended estrous cycle in developing Wistar rats. © 2012 Wiley Periodicals, Inc. Environ Toxicol 29: 814–828, 2014.

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